Noninvasive identification of limited coronary flow reserve in hypertrophic cardiomyopathy

Background Exercise stress testing and dipyridamole infusion induce ischemic-like ST-segment depression in some of the patients with hypertrophic cardiomyopathy. The precise pathophysiologic meaning of these stress-induced ECG changes still appears elusive. The aim of this study was to assess the pathophysiologic meaning of these ECG changes. Methods A high-dose dipyridamole test (two-dimensional echocardiographic and 12-lead ECG monitoring during dipyridamole infusion up to 0.84 mg/kg over 10 minutes) was performed in 22 patients with hypertrophic cardiomyopathy. In addition, regional myocardial blood flow was measured by means of 13N-ammonia and dynamic positron emission tomography in all patients at baseline and after intravenous dipyridamole (0.56 mg over 4 minutes). Results After high-dose dipyridamole testing, seven of 22 patients (responders) had ST-segment depression over 0.2 mV from baseline while 15 of 22 (nonresponders) did not. However, echocardiographic monitoring during dipyridamole testing did not show regional or global dysfunction in any patient. Responders and nonresponders showed comparable values of septal thickness (19 ± 1.6 vs 20 ± 0.9 mm, P is not significant), posterior free wall thickness (10 ± 0.6 vs 10 ± 0.2 mm, P is not significant) and left ventricular end-diastolic diameter (45 ± 2 vs 46 ± 1.6 mm, P is not significant). Coronary vasodilator reserve (dipyridamole/baseline) was lower in responders than in nonresponders both in the septum (1.11 ± 0.30 vs 1.72 ± 0.53, P < 0.01) and in the left ventricular free wall (1.36 ± 0.39 vs 1.93 ± 0.73, P=0.07). Coronary angiography performed in responders showed normal coronary arteries in all of them. Conclusions The ST-segment depression elicited by dipyridamole in patients with hypertrophic cardiomyopathy is associated with a depressed coronary flow reserve even in the absence of angiographically detectable coronary artery disease. The flow reserve seems to be reduced also in nonhypertrophied myocardium, suggesting a primary vascular abnormality.